Timing of Apheresis — Complete Remission Rates
The most clinically important finding from the 2025 multicenter study is the dramatic impact of treatment timing on outcomes. The following data are from Schwake et al. (JNNP, 2025), analyzing 117 apheresis interventions across 571 MOGAD attacks:
Clinical Implication: Unlike most neuroinflammatory conditions where apheresis is reserved as second-line rescue after steroid failure, the evidence in MOGAD suggests that first-line apheresis — initiated concurrently with or instead of steroids — produces dramatically superior outcomes. Clinicians managing acute MOGAD attacks should consider early apheresis consultation rather than waiting for steroid failure.
What is MOGAD?
Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) is a distinct autoimmune demyelinating condition of the central nervous system characterized by the presence of serum antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG). It was historically grouped with Neuromyelitis Optica Spectrum Disorder (NMOSD) due to clinical overlap, but is now recognized as a separate entity with distinct pathophysiology, clinical features, treatment responses, and prognosis.
MOGAD primarily affects the optic nerves (optic neuritis), spinal cord (transverse myelitis), and brain (ADEM-like presentations). Unlike AQP4-IgG positive NMOSD, MOGAD tends to have a better recovery from individual attacks but can cause cumulative disability with repeated relapses. The MOG antibody targets the extracellular domain of MOG, a protein expressed on the outer surface of myelin sheaths, making it directly accessible to circulating antibodies and complement.
MOGAD vs. AQP4+ NMOSD: Key Distinctions
| Feature | MOGAD (MOG-IgG+) | NMOSD (AQP4-IgG+) |
|---|---|---|
| Target antigen | Myelin oligodendrocyte glycoprotein (MOG) | Aquaporin-4 water channel (AQP4) |
| Cell targeted | Oligodendrocytes (myelin-producing cells) | Astrocytes |
| Sex predilection | Equal M:F ratio | Female predominance (9:1) |
| Attack recovery | Generally better per attack | Often incomplete recovery |
| Lesion pattern | Bilateral optic neuritis, long cord lesions, ADEM-like | Area postrema, long cord lesions, optic neuritis |
| Apheresis response | Strong, especially if early | Moderate (Category II) |
| Maintenance therapy | Not always required; individualized | Long-term immunosuppression required |
Landmark Study: Schwake et al. (JNNP, 2025)
Study Design
Multicenter Retrospective Cohort Study
| Parameter | Detail |
|---|---|
| Citation | Schwake C, et al. J Neurol Neurosurg Psychiatry. 2025;96(7):639–646. doi:10.1136/jnnp-2024-334863 — PMC12322437 |
| Sample size | 117 apheresis interventions analyzed across 571 total MOGAD attacks (multiple centers) |
| Procedures used | Therapeutic plasma exchange (TPE) and immunoadsorption (IA) |
| Overall response | 91% of patients either improved or achieved complete remission following apheresis |
| Complete remission — first-line | 67% when apheresis initiated as first-line therapy (≤2 days from attack onset) |
| Complete remission — second/third-line | 15% when apheresis used after prior treatment failure |
| Key predictor of outcome | Delay to apheresis initiation — the single most important modifiable factor |
| Conclusion | "Apheresis is highly effective in MOGAD when initiated early. Delay beyond 2 days of attack onset is associated with substantially lower complete remission rates." |
Overall Outcomes Across All 117 Interventions
Combined improvement + complete remission = 91%. Note: complete remission rates vary dramatically by timing of initiation (see timing data above).
Clinical Presentations and Apheresis Considerations
| Presentation | Apheresis Role | Notes |
|---|---|---|
| Bilateral optic neuritis | Strong evidence; consider first-line | Vision loss is often severe; early apheresis may prevent permanent visual impairment |
| Transverse myelitis | Strong evidence; consider first-line | MOG-IgG positive TM responds particularly well to apheresis; test MOG-IgG in all TM |
| ADEM-like presentation | Moderate evidence | Often seen in pediatric MOGAD; apheresis after steroid failure or in severe cases |
| Brainstem/cortical involvement | Limited evidence | Case reports; consider in severe steroid-refractory cases |
| Relapsing disease | Per-attack treatment | Each attack treated individually; long-term maintenance apheresis not established |
Procedure Protocol
| Parameter | Recommendation |
|---|---|
| Procedure type | TPE or immunoadsorption (IA); both effective in available data |
| Timing | Initiate as early as possible — ideally within 2 days of attack onset for first-line use |
| Number of sessions | 5–7 sessions; individualized based on clinical response |
| Volume per session (TPE) | 1.0–1.5 plasma volumes per session |
| Replacement fluid (TPE) | 5% albumin; FFP if coagulopathy present |
| Concurrent therapy | High-dose IV methylprednisolone (1g/day × 5 days) typically given concurrently or sequentially |
| Monitoring | Clinical neurological assessment after each session; MOG-IgG titers (not required to guide acute treatment) |
| Relapse management | Repeat apheresis for each attack; consider long-term immunosuppression (rituximab, mycophenolate) to prevent relapses |
Proposed ASFA Classification
Note: MOGAD was not listed as a separate indication in the ASFA 9th Edition (2023). The following classification reflects the current evidence base and anticipated ASFA 10th Edition categorization based on the 2025 Schwake et al. data.
The evidence supports apheresis as an accepted treatment for acute MOGAD attacks, with a strong signal for superior outcomes when used early. The retrospective design of available studies limits the evidence grade, but the magnitude of benefit and the absence of effective alternatives in severe attacks supports a Category II designation.
Information for Patients
If you have MOGAD and are experiencing an attack:
MOGAD is a condition where your immune system makes antibodies that attack the insulation around your nerve fibers. This can cause vision loss, weakness, or other neurological symptoms during attacks.
Plasma exchange (plasmapheresis) is a procedure that removes these harmful antibodies from your blood. Research shows it works best when started as early as possible — ideally within the first 2 days of an attack. If you are experiencing a new MOGAD attack, ask your neurologist about plasma exchange right away.
The procedure is generally safe and well-tolerated. A study of 117 treatments showed that 91% of patients improved or went into complete remission after plasma exchange.
References
All references verified February 2026. DOIs and PubMed IDs confirmed against publisher records. Links open in a new tab.
- 1. Schwake C, Ladopoulos T, Häußler V, Kleiter I, Ringelstein M, Aktas O, et al. Apheresis therapies in MOGAD: a retrospective study of 117 therapeutic interventions in 571 attacks. J Neurol Neurosurg Psychiatry. 2025;96(7):639–646. doi:10.1136/jnnp-2024-334863 — PubMed 39496464 — PMC12322437 Free PMC Article
- 2. Jarius S, Paul F, Aktas O, Asgari N, Dale RC, de Seze J, et al. MOG encephalomyelitis: international recommendations on diagnosis and antibody testing. J Neuroinflammation. 2018;15(1):134. doi:10.1186/s12974-018-1144-2 — PubMed 29724224 Free PMC Article
- 3. Cobo-Calvo A, Ruiz A, Maillart E, Audoin B, Zephir H, Bourre B, et al. Clinical spectrum and prognostic value of CNS MOG autoimmunity in adults. Neurology. 2018;90(22):e1858–e1869. doi:10.1212/WNL.0000000000005560 — PubMed 29695592
- 4. Connelly-Smith L, Alquist CR, Aqui NA, Hofmann JC, Klingel R, Onwuemene OA, et al. Guidelines on the Use of Therapeutic Apheresis in Clinical Practice — Evidence-Based Approach from the Writing Committee of the American Society for Apheresis: The Ninth Special Issue. J Clin Apher. 2023;38(2):77–278. doi:10.1002/jca.22043 Free Full Text — PubMed 37017433
- 5. Lu W, Costa V, Wu DW, Alsammak M, Banez-Sese G, Chhibber V, et al. An Annual Review of Important Apheresis Articles in 2024 From the American Society for Apheresis Attending Physician Subcommittee. J Clin Apher. 2025;40(6):e70067. doi:10.1002/jca.70067 Abstract Only — PubMed 41157887
Disclaimer: This information is for educational purposes only. Clinical decisions require individualized assessment by qualified medical professionals. MOGAD is a rapidly evolving field; consult current literature and a neuroimmunology specialist for complex cases.